The mechanism of neuroprotective effect of against serum/glucose deprivation-induced PC12 cell death.

Objective: Oxidative stress is associated with the pathogenesis of brain ischemia and other neurodegenerative disorders. Previous researches have shown the antioxidant activity of   L. In this project, we studied neuro-protective and reactive oxygen species (ROS) scavenging activities of methanol (MeOH) extract and other fractions isolated from in PC12 cell line in serum/glucose deprivation (SGD) condition.

Materials And Methods: The PC12 neuronal cells were pretreated for 6 hr with MeOH extract and fractions of (1 to 25 μg/ml) followed by 24 hr incubation under SGD condition. Cell viability was measured by Alamar Blue assay. The level of ROS was calculated using DCFH-DA. Also, Bax/Bcl-2 protein ratio was analyzed by western blot assay.

Results: SGD condition significantly decreased cells viability (p<0.001). Pretreatment with EtOAc (12.5 and 25 µg/ml), BuOH (12, 25, 50 µg/ml) and CHCl (1.5 µg/ml) fractions of reduced SGD-induced cytotoxicity. MeOH extract could not increase the viability significantly. All four semi polar fractions (EtOAc, BuOH, CH2Cl2 and MeOH) decreased SGD-induced ROS production and changed Bax/Bcl-2 ratio.

Conclusion: showed promising effects against SGD condition; further mechanistic and clinical studies are warranted before application of as a neuro-protective agent.